I dont know is right enough, for them. Those who want to investigate psychobabble dont bother me too terribly, morally or emotionally or whatever. But if they are "certain" they certainly do. If they opine without being able to address physiogenic theories at a high level, they certainly do.

This became a really awesome discussion. I wish I were feeling smart enough at the moment to say much that would really add to it.

is naive about philosophy and the philosophy of science and the bounds of science.

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I find this actually quite a common problem among scientists I have known. Not all of them, surely, but many. Science itself is a philosophy that works really, really well within its particular framework, tells us things about the observable, repeatable world that we would never figure out by other means or methods. But if you step outside of that framework and still try to apply its logic, it can all go to hell really fast, suddenly you're saying things that may seem to have support on the surface but that contain so many underlying assumptions and faulty pieces of logic that you're screwed. That's fine, of course -- it happens. It's that it happens and so many people don't recognize it happening, and instead hold on to it as "scientific", that's really disturbing.

Pain is a perception. It doesn't exist otherwise. That's true whether it's triggered from an obvious outside physical source or no. So saying that somebody has the perception of pain, implying that it isn't "real" pain, is either a totally sloppy way of saying a physical stimulus that we've generally associated with the pain response is absent, or it's a total misunderstanding of perception itself. If it's the former, that doesn't mean much -- we don't see a physical, outside source of the pain in many neurological diseases. Pain is triggering "inappropriately", not in response to an outside stimulus, but that doesn't make it not pain, and it doesn't make it psychogenic, at least any moreso than any perception is psychogenic. If it's the latter, it's frustrating that somebody who obviously doesn't understand perception is so involved in research that inherently involves disturbances in perception.

"I don't know" is the most valuable phrase any scientist or doctor can ever learn, I think. Knowing what can and can't be known for sure is important, and understanding what the data isn't telling you is every bit as important as seeing clearly what it is telling you. In fact, if you don't have an understanding of both, you don't have an understanding of either.

Just to be the pedant that I am, note that "psychological" is certainly a fair description of say depression, in the abstract, if one sets aside how the word might be mis-perceived. But in practice, everyone mis-perceives it!

Everyone perceives that it means these illnesses have a psychological origin or cause, not merely a psychological nature. But that is not established. I am one who believes it likely that no psychogenic diseases exist, except maybe PTSD. Many groups including some in high places (Harvard) find that elevated cytokines are a likely cause of major depression; however this is hotly disputed.

Of course, in science we assume without overwhelming proof that the psyche is made of neurons and their actions, because there is no way to address the psyche scientifically if this isnt so. I still believe that a fairly clear distinction between psychogenic and physiogenic can be made. The former occurs via experiences, via what comes into the "psyche" and how it is processed. An event in the psyche should precede any physical change that can be summarized in the sense of "a great percentage of dopaminergic neurons in the substantia nigra died". The physical changes that correspond to an event in the psyche presumably lack this simplicity; they should instead contain incompressible information such as "this neuron fired, then this one and this one, and 25 milliseconds later, this one did", etc.

I do think that a pyschogenic disease, if any exist, could cause summarizable, compressible physical events that are causally downstream of the disease cause. For example, depression *could* be psychogenic, and the psyche could, eventually, cause the elevated cortisol found in something like 1/2 of depression patients. The cortisol change could even be upstream of the depression experience (altered qualia and behavior). But only a psychological-neural phenomenon with no simple physical description can be at the top, if it be a psychogenic disease. If a great percentage of dopaminergic neurons in the substantia nigra die, this too could have a psychological cause -- but only if the less-compressible psychological phenomenon happens first.

So yeah, depression-ologists often take depression to be psychogenic and yet to very often show elevated cortisol. Lloyd is doing the same thing they are doing. The only absolute reason to believe that Parkinson's disease is *not* psychogenic is because the correlated physical phenomenon (death of dopaminergin neurons in the substantia nigra) is more spectacular than elevated cortisol.

Actually there is one more reason. Most diseases lower fitness and there should, ideally, be some reason why they occur nevertheless. I think many people find it easier to see how psychogenic depression could happen nevertheless, and cant see why psychogenic Parkinson's could happen nevertheless. I dont really agree, but it would take another page or two to explain.

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Ah, the old nature-nurture debate. The 'adaptive' mechanisms of the brain do indeed include a type of neural network learning process that by definition means that cognitive events can produce biological change in an organism. Therefore, the trigger of a 'brain restructuring event' may be purely psychological, emotional, or even a traumatic fantasy, but if that event persistes long enough, and if it occurs during critical periods in the brain's development ( there may be many throughout life), the neural connections that result may persist indefinitely. In other words, the brain is like a computer that can be re-wired every day, resulting in a hardware 'trace' of our thoughts and actions that will persist and indirectly influence how we are able to adapt and respond in the future. And if the adaptation is dysfunctional (auto-stressing the organism), immune functions can be seriously compromised, inviting in certain chronic infections that are stress-responsive (such as HHV).

On the other hand, biological traumas can also trigger the brain's adaptive mechanisms. I particularly like the viewpoint on CFS put forward by Dr Bell, who views CFS as a post-infectious dysautonomia. In other words, an infection re-programs the neural network in a way that it can not longer keep HPA balance. Primarily this is probably the hypothalamus being re-wired by an overwhelming or dysfunctional immune response. The bug itself may be long gone, or may be held mostly in remission, but the dysautonomia remains because it has become hard-wired into the brain. And this dysautonomia leads to immune imbalances that invite new co-infections to take hold over time.

So either situation, psychogenic or physiologic, could conceivably lead to dysautonomia, and perhaps in some cases both occur, which might create a strong vicious cycle. Certainly this happens with depression, it can clearly be caused by either psychological or physical factors, or both. And probably one common physical cause of depression is digestive dysbiosis and leaky gut which lowers serotonin production. But those can probably also be the result of prolonged trauma also, because the FF response lowers bloodflow to the gut. So we have this constant interplay between the cognitive and the physical elements of our being.

Personally I expect that CFS and its close sibling illnesses will eventually take a unique place in medicine, I believe there is an entire category of dysautonomia illnesses, basically a hypothalamic dysfunction spectrum disorder. All the different ways to create dysautonomia, all the various ways to overwhelm the hypothalamus. And so treatments should be coordinated to address all the pathologies involved, somewhat holistic. This requires a lot of ongoing diagnostic work...

What options do scientists have if XMRV is not the causative agent? Since XMRV is now outside of our locus of control, I hope someone could speculate on other causes or treatments.

-Fertilizing the ovaries of chinese hamsters and culturing them in the blood/CSF of CFIDS patients and healthy controls, then implanting them in utero. Screen for antibodies produced by the offspring and develop a chimeric autoantibody based on the results.

Here is the article about fibromyalgia and Lyrica. Sounds familiar, doesn't it?

Drug Approved. Is Disease Real?

By ALEX BERENSON
Published: January 14, 2008

Fibromyalgia is a real disease. Or so says Pfizer in a new television advertising campaign for Lyrica, the first medicine approved to treat the pain condition, whose very existence is questioned by some doctors.

For patient advocacy groups and doctors who specialize in fibromyalgia, the Lyrica approval is a milestone. They say they hope Lyrica and two other drugs that may be approved this year will legitimize fibromyalgia, just as Prozac brought depression into the mainstream.

But other doctors including the one who wrote the 1990 paper that defined fibromyalgia but who has since changed his mind say that the disease does not exist and that Lyrica and the other drugs will be taken by millions of people who do not need them.

As diagnosed, fibromyalgia primarily affects middle-aged women and is characterized by chronic, widespread pain of unknown origin. Many of its sufferers are afflicted by other similarly nebulous conditions, like irritable bowel syndrome.

Because fibromyalgia patients typically do not respond to conventional painkillers like aspirin, drug makers are focusing on medicines like Lyrica that affect the brain and the perception of pain.
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Despite the controversy, the American College of Rheumatology, the Food and Drug Administration and insurers recognize fibromyalgia as a diagnosable disease. And drug companies are aggressively pursuing fibromyalgia treatments, seeing the potential for a major new market.
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But doctors who are skeptical of fibromyalgia say vague complaints of chronic pain do not add up to a disease. No biological tests exist to diagnose fibromyalgia, and the condition cannot be linked to any environmental or biological causes.
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Dr. Frederick Wolfe, the director of the National Databank for Rheumatic Diseases and the lead author of the 1990 paper that first defined the diagnostic guidelines for fibromyalgia, says he has become cynical and discouraged about the diagnosis. He now considers the condition a physical response to stress, depression, and economic and social anxiety.
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When you help physicians to recognize the condition and you give them treatments that are well tolerated, you overcome their reluctance, he said.
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Theres definitely room for several drugs, Dr. Chappell said.

But physicians who are opposed to the fibromyalgia diagnosis say the new drugs will probably do little for patients. Over time, fibromyalgia patients tend to cycle among many different painkillers, sleep medicines and antidepressants, using each for a while until its benefit fades, Dr. Wolfe said.

The fundamental problem is that the improvement that you see, which is not really great in clinical trials, is not maintained, Dr. Wolfe said.

Still, Dr. Wolfe expects the drugs will be widely used. The companies, he said, are going to make a fortune.

The 'adaptive' mechanisms of the brain do indeed include a type of neural network learning process that by definition means that cognitive events can produce biological change in an organism...

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Kurt,

What you are discussing is a hypothetical model in "neural networking", itself a field of theoretical modeling in what is called "cognitive science", which melds studies of computer science, linguistics, psychology, and neurobiology. Very few people who work in cognitive science have MDs, apart from psychiatrists, and in fact when I was studying in that area many didn't even have bachelor's degrees in biology. Although neural networking models have been employed in neuroscience, they remain strictly hypothetical at best. There is scant evidence as yet for the psychogenic causation of CNS dysfunction on the scale you have stated. Certainly there is no proof that psychological factors can cause observable CNS damage. There is however abundant proof that pathogens, toxins, and immune responses can cause CNS damage or merely persistent dysautonomia.

Lloyd and others who seem at least tangentially connected with particular psychological researchers (White and Wessely in the UK, some of the Emory University psychiatrists in the US) are among the influential few who continue to research this model, which is growing in popularity with segments of the psychiatric community who have a very unscientific view of "somatization disorders"; see the many links in the DSM vs WHO thread. That in itself does not invalidate their research, but their frequently distorted presentations are problematic, to say the least. They have a tendency to overstate the scientific validity of their speculative model and to downplay or ignore the extensive research findings on physical causation of the phenomena they are studying.

This allows for some very poor science, such as the all-too-hasty embrace of a 'holistic' model of illness centered conveniently on the HPA axis (one of the few CNS interfaces between multiple systems that has been closely studied and that is clearly involved in certain emotional responses); this model as you described it above will sound very familiar to many because it is the same one that has been employed to "explain" CFS since the advent of psychosomatic theories of CFS in the late 80's/early 90's. But giving "psychogenesis" the same or similar weight as organic causes of CNS dysregulation or damage is not scientifically sound at this point, especially not in ME/CFS studies, which have found quite the opposite: that ME/CFS patients have CNS pathology (hypoperfusion patterns, glucose metabolism, brainwave patterns, microglial activity, etc) that is distinct from that seen in known psychiatric conditions alone, even those frequently seen co-morbid with CFS.

In a perfect world, scientific research would always be objective, but in reality it often is not. Different researchers bring their own biases, of course, but unfortunately many areas are also highly politicized - like CFS research. This gives us the additional burden of having to sift through research with almost the same caution we would bring to a historical discussion, instead of with the "face-value" approach that assumes researchers are operating objectively and giving us the whole picture. I have a background in neurobiology and have been consistently disturbed over the years by the flawed premises and lack of scientific rigor in the studies on 'psychobiology' of ME/CFS. My professors would have shot down most of these studies at the time they were first proposed.

I am MOST interested in the Kerr study and how XMRV and our genes MAY be connected. I am concerned about the genetics of this disease because of siblings and a very smart 9 year old niece and a very smart 8 month old nephew. I would rather have 15 cancers, one after another, than see either of these beautiful kids live my life. So, Kerr and his gene study is critical to me.

I'm with you, muffin...I have a 21 y.o. grdau with CFS since age 14. She just came to live with me as she was destitute, unable to care for herself, and with no health insurance or ability to fend for herself and fill out forms for SSDI/SSI. I'm doing that now and have good dr. for her. I also have one daughter with slight signs of CFS, and a briliant 12 y.o. grson that so far seem very well and healthy.

Note, on co-cure today, they broadcast a replication study in the UK that found NO XMRV in any tested; however, they also used a group of their 'unwell' patients (who could have anything in the world, not real CFS/ME), and did not use the stringent methodology that the Wittemore Peterson Institute did, AND one of the so-called 'researchers' was of the psychobabble group, Dr. Simon Wesselly.
Did you know the UK has a ban on M.E files of the government being opened until something like 2035 or later? Very interesting.

The more I read and learn, the more I know good scientists are very interested in this new retrovirus and are studiously trying to replicate the pilot study in CFS. One can only wait and be patient and hope.
Dr. Judy Milovits, the lead scientist on the pilot study, worked for 22 years at the National Cancer Institute, and knows her retroviruses very well, will be giving a video broadcast on Jan 22 about the further work taking place. Should be interesting.

I wanted to comment on the previous comments about Lloyd's XMRV studies in Australia.

I read the 2006 paper and also the commentary related to it when it was released.

One point that has stood out to me about the Dubbo study is that really, when it came down to it, they only had N=20-odd patients with CFS so it was a very small sample size. (10% of 200-odd patients developed CFS)

Secondly, if XMRV studies are replicated in this group of 20, is it the right group? Lloyd was quoted as saying that 95% of the group had recovered by 1 year and 99% of the group by 2 years. This is entirely different from what is in the last few decades of CFS literature. Despite using different definitions of CFS, a 2005 Dutch review of prognosis still put the figure at less than 10% full recovery from a multitude of studies using a multitiude of definitions. An 80% discrepancy is too high. A colleague wrote Dr. Lloyd directly to confirm the figures and he did and reiterated it was "full recovery."

Here's an update on two replication studies being done through Gordon Medical Associates.

GMA patients who were tested in either one of two studies need to stay patient a little longer. We have provided over 130 samples to Dr. Judy Mikovits for extended testing for XMRV. Dr. Mikovits tells us most of those samples have been tested, and that we will receive the results as soon as they are finished analyzing the data. Those who provided samples to Panorama labs will also need to wait. XMRV is proving to be a difficult virus to find in testing, and both labs are working to do their best to provide accurate information. We will contact you as soon as we receive the results.